Evidence map›Paper›PMID 24603337›Full record

ArticleCell death & disease2014

Helicobacter pylori sensitizes TNF-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis in human gastric epithelial cells through regulation of FLIP.

W-C Lin, H-F Tsai, H-J Liao, C-H Tang, Y-Y Wu, P-I Hsu, A-L Cheng, P-N Hsu

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.2field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Mitochondrial Stress inAntioxidants (Basel, Switzerland) · 2026
    Review
  2. Article
  3. Review
  4. Frontiers in cell and developmental biology · 2023
    Review
  5. Article
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  14. Review
  15. Distinct roles of TNF-related apoptosis-inducing ligand (TRAIL) in viral and bacterial infections: from pathogenesis to pathogen clearance.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2016
    Review
  16. Role of Helicobacter pylori infection in pathogenesis of gastric carcinoma.World journal of gastrointestinal pathophysiology · 2016
    Review
  17. Review
  18. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 5 institutions in 1 country.

W-C LinGraduate Institute of Immunology, College of Medicine, National Taiwan University, Taipei, Taiwan.
H-F Tsai1] Department of Internal Medicine, Taipei Medical University Shuang Ho Hospital, Taipei, Taiwan [2] Gradute Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
H-J LiaoGraduate Institute of Immunology, College of Medicine, National Taiwan University, Taipei, Taiwan.
C-H TangGraduate Institute of Immunology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Y-Y WuDepartment of Medical Laboratory Science and Biotechnology, China Medical University and Hospital, Taichung, Taiwan.
P-I HsuDepartment of Internal Medicine, Veterans General Hospital-Kaohsiung, Kaohsiung, Taiwan.
A-L Cheng1] Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan [2] Department of Oncology, National Taiwan University Hospital, Taipei, Taiwan.
P-N Hsu1] Graduate Institute of Immunology, College of Medicine, National Taiwan University, Taipei, Taiwan [2] Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
National Taiwan University · TWKaohsiung Veterans General Hospital · TWChina Medical University Hospital · TWNational Taiwan University Hospital · TWTaipei Medical University-Shuang Ho Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Helicobacter pylori (H. pylori) infection is associated with chronic gastritis, peptic ulcer and gastric cancer. Apoptosis induced by microbial infections is implicated in the pathogenesis of H. pylori infection. Here we show that human gastric epithelial cells sensitized to H. pylori confer susceptibility to TRAIL-mediated apoptosis via modulation of death receptor signaling. Human gastric epithelial cells are intrinsically resistant to TRAIL-mediated apoptosis. The induction of TRAIL sensitivity by H. pylori is dependent on the activation of caspase-8 and its downstream pathway. H. pylori induces caspase-8 activation via enhanced assembly of the TRAIL death-inducing signaling complex (DISC) through downregulation of cellular FLICE-inhibitory protein (FLIP). Overexpression of FLIP abolished the H. pylori-induced TRAIL sensitivity in human gastric epithelial cells. Our study thus demonstrates that H. pylori induces sensitivity to TRAIL apoptosis by regulation of FLIP and assembly of DISC, which initiates caspase activation, resulting in the breakdown of resistance to apoptosis, and provides insight into the pathogenesis of gastric damage in Helicobacter infection. Modulation of host apoptosis signaling by bacterial interaction adds a new dimension to the pathogenesis of Helicobacter.

Indexed as

ApoptosisBH3 Interacting Domain Death Agonist ProteinCASP8 and FADD-Like Apoptosis Regulating ProteinCaspase 8Cell Line, TumorCytochromes cDeath Domain Receptor Signaling Adaptor ProteinsDose-Response Relationship, DrugEnzyme ActivationEpithelial CellsGastric MucosaHelicobacter InfectionsHelicobacter pyloriHumansMitochondriaRecombinant ProteinsBH3 Interacting Domain Death Agonist ProteinBID protein, humanCASP8 and FADD-Like Apoptosis Regulating ProteinCASP8 protein, humanCaspase 8CFLAR protein, humanCytochromes cDeath Domain Receptor Signaling Adaptor ProteinsRecombinant ProteinsTNF-Related Apoptosis-Inducing LigandTNFSF10 protein, human

Identifiers

PMID24603337
PMCPMC3973194
OpenAlexW1966821034

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.